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Vitamin E succinate induces Fas-mediated apoptosis in estrogen receptor negative human breast cancer cells

  1. Author:
    Turley, J. M.
    Fu, T.
    Ruscetti, F. W.
    Mikovits, J. A.
    Bertolette, D. C.
    Birchenall-Roberts, M. C.
    1. Year of Conference: 1997
  1. Conference Name: Annual Meeting of the American Association for Cancer Research
    1. 38
    2. Pages: A4197
  2. Type of Work: Meeting Abstract
  1. Abstract:

    Vitamin E succinate (VES), a derivative of the fat soluble vitamin D-alpha-tocopherol (vitamin E), inhibited growth and induced apoptotic cell death of estrogen receptor negative human breast cancer cells. VES induced apoptosis in MDA-MB-231 and SKBR-3 cells occurred through a Fas pathway. Total protein levels of the Fas receptor (Fas; APO-1/CD-95) and the Fas-Ligand (Fas-L) were increased following VES-treatment. In addition, VES increased cell surface Fas expression. Fas- neutralizing antibodies and Fas-L antisense oligonucleotides blocked VES-induced apoptosis. The presence of Fas-L antisense oligonucleotides also completely blocked the VES-mediated increase in Fas-L protein expression. These data indicate a role for Fas-signaling in VES-mediated apoptotic cell death of human breast cancer cells. These data suggest that VES may be of clinical use in the treatment of aggressive human breast cancers, particularly those that are refractory to anti-estrogen therapy.

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